fig2: APC-induced GRP78 expression in the presence and absence of LPS stimulation. Following HUVEC treatment with 150 nM APC for 0, 6, 12, and 24 h, upregulated GRP78 expression was initially detected at 6 h by Western blot analysis (GRP78 (a), P < 0.05), and then generally decreased. After continuous exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h. Upregulated GRP78 expression was also detected at 6 h by Western blot analysis (GRP78 (b), P < 0.05), and then generally decreased. A significant difference in APC-induced GRP78 expression in the presence (b) and absence (a) of LPS stimulation was detected at 6 h, which indicated that 150 nM APC plays a more significant role in this effect following LPS stimulation (P < 0.05).

Mentions:
Evidence has been obtained in previous studies that 150 nM APC induces a transient rise in calcium release from ER in HUVECs, implying an ER disturbance evoked by APC [13]. To investigate ER stress induced by APC, the effect of an ER-stress-related protein, GRP78 on HUVECs was examined following exposure for 0, 6, 12, 24 h. APC treatment upregulated GRP78 protein expression at 6 h (Figure 2). Upregulated GRP78 is responsible for the UPR in the ER. Therefore, these data indicate that APC acts as an ER stressor and elicits the UPR.

fig2: APC-induced GRP78 expression in the presence and absence of LPS stimulation. Following HUVEC treatment with 150 nM APC for 0, 6, 12, and 24 h, upregulated GRP78 expression was initially detected at 6 h by Western blot analysis (GRP78 (a), P < 0.05), and then generally decreased. After continuous exposure to 10 ng/mL LPS for 24 h, HUVECs were treated with 150 nM APC for 0, 6, 12, and 24 h. Upregulated GRP78 expression was also detected at 6 h by Western blot analysis (GRP78 (b), P < 0.05), and then generally decreased. A significant difference in APC-induced GRP78 expression in the presence (b) and absence (a) of LPS stimulation was detected at 6 h, which indicated that 150 nM APC plays a more significant role in this effect following LPS stimulation (P < 0.05).

Mentions:
Evidence has been obtained in previous studies that 150 nM APC induces a transient rise in calcium release from ER in HUVECs, implying an ER disturbance evoked by APC [13]. To investigate ER stress induced by APC, the effect of an ER-stress-related protein, GRP78 on HUVECs was examined following exposure for 0, 6, 12, 24 h. APC treatment upregulated GRP78 protein expression at 6 h (Figure 2). Upregulated GRP78 is responsible for the UPR in the ER. Therefore, these data indicate that APC acts as an ER stressor and elicits the UPR.